Nitric Oxide and Platelet-Mediated Hemostasis

Nitric oxide (NO·) inhibits platelet function by limiting platelet adhesion and aggregation, as well as disaggregating previously aggregated platelets (1–5). Under resting conditions, blood flow stimulates the endothelium to produce NO·, which regulates platelet activity (6–8). NO· activates soluble guanylyl cyclase leading to a concomitant increase in the production of cyclic guanosine monophosphate (cGMP), the principal mediator of NO· s effects. As a consequence of disease states, the amount of NO· being produced by the endothelium and the platelet itself may be adversely altered, resulting in impairment in platelet aggregation and function. In this chapter we provide evidence for the importance of NO· in regulating platelet function and hemostasis, and we also illustrate the role of NO· deficiency in thrombotic disease.